Lipid metabolism and steatohepatitis development in patients with nonalcoholic fatty liver disease and arterial hypertension

Abstract

Introduction. Dyslipidemia is one of the pathogenetic mechanisms of comorbidity of nonalcoholic fatty liver disease (NAFLD) and hypertension (HTN). Lipid infiltration of hepatocytes is a primary component of steatosis development and lipid metabolism disruption in these patients, while more intense inflammation in steatohepatitis causes a decrease in their levels. Objective: to investigate the relationship between lipid content and the intensity of liver damage in patients with NAFLD and concomitant HTN. Materials and methods. The main group — 49 patients (67.3% women and 32.7% men) with NAFLD and HTN; the comparison group — 51 patients with isolated NAFLD (58.8% women and 41.2% men), the control group — 20 people (55.0% women and 45.0% men). The median age, respectively, was 51.0 [45.0; 56.0] years (p=0.980), 52.0 [47.0; 54.0] years (p=0.610) and 51.0 [45.0; 55.5] years (p=0.564). The body mass index (BMI) was calculated according to the standard method according to the formula: the ratio of body weight in kilograms to height in meters squared: BMI = body weight, kg/height, cm2. Among the main group, 27 (55.1%) patients had steatosis, 22 (44.9%) patients had steatohepatitis. In the comparison group, there were 30 (58.8%) and 21 (41.2%) (p = 0.707), respectively. The levels of total cholesterol (TC), low density lipoproteins (LDL) and very low density lipoproteins (VLDL) were determined using the enzymatic colorimetric method The diagnosis of NAFLD and HTN was established in accordance with local and international recommendations and guidelines. Ultrasound examination was carried out according to the standard method on an empty stomach on a Samsung (Medison) SonoAce X8 device. Two groups of several indicators were compared by the Mann-Whitney test. Logistic regression was applied to identify predictors and prediction models. IBM SPSS 25.0 for Windows was used for statistical calculations. Results. The median BMI of the main group was 27.8 [26.6; 28.5] kg/m2; in the comparison group — 27.3 [24.2; 28.3] kg/m2, which was significantly (p<0.001) higher than in the control group (24.3 [21.9; 26.0] kg/m2). Median TC levels in patients with NAFLD+HTN and steatohepatitis were 5,1 [4,5; 5,5] µ/l, steatosis 6,2 [5,4; 7,1] µ/l (р≤0,001), in patients with isolated NAFLD and steatohepatitis 5,4 [4,9; 6,2] µ/l, steatosis 5,4 [4,9; 6,2] µ/l (р≤0,05). Median LDL levels in the main group with steatohepatitis were 3,4 [3,0; 3,6] µ/l, steatosis 3,9 [3,2; 5,1] µ/l (р≤0,001), in the comparison group with steatohepatitis 2,9 [2,6; 3,3] µ/l, steatosis 3,3 [2,6; 3,8] µ/l (р≤0,05). Median VLDL in NAFLD+HTN group and steatohepatitis were 0,56 [0,47; 0,61] µ/l, steatosis 0,82 [0,77; 0,84] µ/l (р≤0,05), in isolated NAFLD group and steatohepatitis were 0,52 [0,44; 0,68] µ/l, steatosis 0,62 [0,47; 0,67] µ/l (р≤0,05). According to univariate analysis the higher levels of LDL (OR = 0.662 [95.0% CI 0.410–1.069], p = 0.092) and VLDL (OR = 0.003 [95.0% CI 0.001–0.061], p < 0.001) were associated with a lower steatohepatitis probability. At the same time, in the multivariate analysis, the presence of concomitant hypertension showed a significant relationship with the steatohepatitis development in patients with NAFLD (OR = 0.334 [95.0% CI 0.121–0.925], p = 0.035) Conclusions. A reliable inverse association of elevated LDL and VLDL levels with the steatohepatitis presence in patients with NAFLD was determined, while concomitant hypertension was a reliable predictor of its development. The results indicate a close relationship between dyslipidemia and increased systemic pressure with the intensification of liver parenchymal damage in patients with NAFLD.